Evidence map›Paper›PMID 32176643›Full record

ArticleJournal of Alzheimer's disease : JAD2020

Cerebrospinal Fluid Biomarkers in Cerebral Amyloid Angiopathy.

Gargi Banerjee, Gareth Ambler, Ashvini Keshavan, Ross W Paterson, Martha S Foiani, Jamie Toombs, Amanda Heslegrave, John C Dickson, Francesco Fraioli, Ashley M Groves and 5 more

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06960538 (PRIORITY), which is not on this map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT06960538 completednot on this mapstarted 2021, after this paper: background citation

PRIORITY (Enpowering Progression Risk of Cerebral Amyloid Angiopathy)

TypeobservationalSponsorFondazione I.R.C.C.S. Istituto Neurologico Carlo BestaRan2021 to 2025Enrolled200ConditionsCerebral Amyloid Angiopathy, CAA - Cerebral Amyloid Angiopathy
3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Prevalence of cerebral amyloid angiopathy: A systematic review and meta-analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022
    Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Identifying subphenotypes of patients undergoing post-operative delirium assessment.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Observational
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Fluid biomarkers in cerebral amyloid angiopathy.Frontiers in neuroscience · 2024
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 2 countries.

Gargi BanerjeeStroke Research Centre, Department of Brain Repair and Rehabilitation, UCL Queen Square Institute of Neurology and the National Hospital for Neurology and Neurosurgery, London, UK.
Gareth AmblerDepartment of Statistical Science, University College London, Gower Street, London, UK.
Ashvini KeshavanDementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK.
Ross W PatersonDementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK.
Martha S FoianiDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK.
Jamie ToombsDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK.
Amanda HeslegraveDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK.
John C DicksonInstitute of Nuclear Medicine, UCL and University College Hospital, London, UK.
Francesco FraioliInstitute of Nuclear Medicine, UCL and University College Hospital, London, UK.
Ashley M GrovesInstitute of Nuclear Medicine, UCL and University College Hospital, London, UK.
Michael P LunnDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK.
Nick C FoxDementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK.
Henrik ZetterbergDepartment of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK.
Jonathan M SchottDementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK.
David J WerringStroke Research Centre, Department of Brain Repair and Rehabilitation, UCL Queen Square Institute of Neurology and the National Hospital for Neurology and Neurosurgery, London, UK.
UK Dementia Research Institute · GBNational Hospital for Neurology and Neurosurgery · GBUniversity College Hospital · GBSahlgrenska University Hospital · SEUniversity College London · GB

Funding

REGULATION OF COLLAGENASE 3 GENE EXPRESSION BY CYTOKINESK08AR002012 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI RAHMAN, MAHBOOB U · 1998 to 2002
$374k
ALTERNATIVE PATHWAYS OF T CELL ACTIVATIONK08AR002017 · NIAMS · VANDERBILT UNIVERSITY · PI BYRD, VICTOR M · 1998 to 2002
$348k
Arthritis Research UK ARUK-NETWORK 2012-6-ICEArthritis Research UK ARUK-PG2017-1946British Heart FoundationDepartment of HealthMedical Research Council MR/L023784/1
6 · The paper itself

Abstract

backgroundThere is limited data on cerebrospinal fluid (CSF) biomarkers in sporadic amyloid-β (Aβ) cerebral amyloid angiopathy (CAA).

objectiveTo determine the profile of biomarkers relevant to neurodegenerative disease in the CSF of patients with CAA.

methodsWe performed a detailed comparison of CSF markers, comparing patients with CAA, Alzheimer's disease (AD), and control (CS) participants, recruited from the Biomarkers and Outcomes in CAA (BOCAA) study, and a Specialist Cognitive Disorders Service.

resultsWe included 10 CAA, 20 AD, and 10 CS participants (mean age 68.6, 62.5, and 62.2 years, respectively). In unadjusted analyses, CAA patients had a distinctive CSF biomarker profile, with significantly lower (p < 0.01) median concentrations of Aβ38, Aβ40, Aβ42, sAβPPα, and sAβPPβ. CAA patients had higher levels of neurofilament light (NFL) than the CS group (p < 0.01), but there were no significant differences in CSF total tau, phospho-tau, soluble TREM2 (sTREM2), or neurogranin concentrations. AD patients had higher total tau, phospho-tau and neurogranin than CS and CAA groups. In age-adjusted analyses, differences for the CAA group remained for Aβ38, Aβ40, Aβ42, and sAβPPβ. Comparing CAA patients with amyloid-PET positive (n = 5) and negative (n = 5) scans, PET positive individuals had lower (p < 0.05) concentrations of CSF Aβ42, and higher total tau, phospho-tau, NFL, and neurogranin concentrations, consistent with an "AD-like" profile.

conclusionCAA has a characteristic biomarker profile, suggestive of a global, rather than selective, accumulation of amyloid species; we also provide evidence of different phenotypes according to amyloid-PET positivity. Further replication and validation of these preliminary findings in larger cohorts is needed.

Indexed as

AgedAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorBiomarkersCase-Control StudiesCerebral Amyloid AngiopathyFemaleHumansMaleMiddle AgedNeurofilament ProteinsPeptide Fragmentstau ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)amyloid beta-protein (25-38)Amyloid beta-Protein PrecursorBiomarkersneurofilament protein LNeurofilament ProteinsPeptide Fragmentstau ProteinsAlzheimer’s diseaseamyloid-βbiomarkerscerebral amyloid angiopathycerebrospinal fluid

Identifiers

PMID32176643
PMCPMC7242825
OpenAlexW3012005832

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.